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Plants face various pathogen challenges. Pathogen infection can not only trigger local defence responses to restrict pathogen growth at the primary infection sites, it can also induce plants to generate mobile signals, which move to the uninfected tissue to protect them from further pathogen attack. This primed immunity is called systemic acquired resistance (SAR). A SAR defective mutant fmo1 was identified for a long time, whereas its function was uncovered recently to be an enzyme generating a novel molecule called N-hydroxy-pipecolic acid (NHP). External application of NHP on the root of fmo1 could be detected in distal leaves and restore the SAR defects of fmo1, which suggests that NHP or its derivatives may act as the SAR mobile signal. However, it is unclear how NHP or its derivatives is transported. Considering that NHP is an amino acid metabolite and is derived from Lysine, we hypothesized that the non-selective amino acid transporter Glutamine dumpers (GDUs) may play some roles in NHP or its derivatives transport. In my PhD, I did reverse genetic study of the GDU family. We generated the gdu1/2/3/4 quadruple mutant and its SAR response was a bit suppressed, which suggests that GDUs may have function in regulating SAR. For my exchange, I hope to answer the question what signal(s) are transported by GDUs in SAR. We plan to do the non-targeted metabolomics analysis of the phloem extrudates of GDUs to see if there is any NHP or NHP derivatives. If some new NHP derivative is found, we can design feeding experiment to test its function in SAR. This will further our understanding of the role of NHP in SAR.
Xin Li
Georg-August-Universität Göttingen
Life Sciences
Education
The University of British Columbia
Globalink Research Award
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